PROTEOMIC ALTERATION OF 16HBE14O- HUMAN BRONCHIAL EPITHELIAL CELLS AFTER INFECTION BY BORDETELLA PERTUSSIS

GESELL SALAZAR, MANUELA; CARRICA, MARIELA; LAMBERTI, YANINA; BAROLI, CARLOS; SCHMIDT, FRANK; BAROLI, CARLOS; SCHMIDT, FRANK; DEBANDI, MARTINA; HENTSCHKER, CHRISTIAN; RODRIGUEZ, MARIA EUGENIA; DEBANDI, MARTINA; HENTSCHKER, CHRISTIAN; RODRIGUEZ, MARIA EUGENIA; GESELL SALAZAR, MANUELA; CARRICA, MARIELA; LAMBERTI, YANINA

Simposio; 12th International Symposium on Bordetella; 2019

The airway epithelium is considered central to the orchestration of pulmonaryinflammatory and is critically involved in the regulation of immune responses. Previous studies indicated that B. pertussis (Bp) is able to enter and survive in compartments with early-endosomes characteristics in respiratory epithelial cells suggesting that this pathogen have developed strategies to exploit host functions for survival. Pertussis toxin (PT) plays a major role in the modulation of host responses. Here, we focused on host proteome alterations induced by Bp in epithelial cells in order to better understand this interaction. To this end, the cell line 16HBE14o- (provided by Dr. Cozens), which retains characteristic features of primary bronchial epithelial cells, were infected with Bp wild type or an isogenic mutant lacking PT during 4.5 h and 8 h at a multiplicity of infection of one. Host cell response was compared to a similarly treated uninfected control. LC-MS/MS in data independent adquisition mode (DIA) allowed the identification of 2854 host proteins. The abundance level of 719 proteins were significantly altered by Bp infection compared with the control (p